Fig. 8: Proposed mechanisms of the D1–D2DR heteromer-mediated signaling pathway in neuropathic pain. | Experimental & Molecular Medicine

Fig. 8: Proposed mechanisms of the D1–D2DR heteromer-mediated signaling pathway in neuropathic pain.

From: The dopamine D1–D2DR complex in the rat spinal cord promotes neuropathic pain by increasing neuronal excitability after chronic constriction injury

Fig. 8

Activation of the D1–D2DR heteromer leads to intracellular calcium mobilization from IP3 receptor-sensitive stores through a cascade of events involving rapid translocation of Gαq to the plasma membrane and activation of PLC. The increase in the calcium concentration leads to the promotion of PKC γ, CaMKII, MAPK, and CREB activation, which could increase the excitability of spinal neurons to promote the development of chronic neuropathic pain. l-CDL inhibits the formation of the D1–D2DR complex and downstream PKC γ, CaMKII, MAPK, and CREB signaling to alleviate CCI-induced neuropathic pain.

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